Evidence map›Paper›PMID 34424346›Full record

ReviewCellular and molecular life sciences : CMLS2021

Chemotherapy-induced cognitive impairment: focus on the intersection of oxidative stress and TNFα.

Nicole G Rummel, Luksana Chaiswing, Subbarao Bondada, Daret K St Clair, D Allan Butterfield

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Cancer treatment-related cognitive impairment.Neuro-oncology advances · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Chemotherapy-related cognitive impairment and kidney dysfunction.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Chemobrain: An accelerated aging process linking adenosine AInternational review of neurobiology · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Nicole G RummelDepartment of Chemistry, University of Kentucky, Lexington, KY, 40506, USA.
Luksana ChaiswingMarkey Cancer Center, University of Kentucky, Lexington, KY, 40536, USA.
Subbarao BondadaMarkey Cancer Center, University of Kentucky, Lexington, KY, 40536, USA.
Daret K St ClairMarkey Cancer Center, University of Kentucky, Lexington, KY, 40536, USA.
D Allan ButterfieldDepartment of Chemistry, University of Kentucky, Lexington, KY, 40506, USA. dabcns@uky.edu.ORCID http://orcid.org/0000-0003-3254-5286
University of Kentucky · US

Funding

(PQ9)A redox-mediated mechanism of chemotherapy-induced cognitive impairmentR01CA217934 · NCI · UNIVERSITY OF KENTUCKY · PI BONDADA, SUBBARAO, BUTTERFIELD, D. ALLAN · 2017 to 2021
$2.7M
NCI NIH HHS R01 CA217934
6 · The paper itself

Abstract

Chemotherapy-induced cognitive impairment (CICI) has been observed in a large fraction of cancer survivors. Although many of the chemotherapeutic drugs do not cross the blood-brain barrier, following treatment, the structure and function of the brain are altered and cognitive dysfunction occurs in a significant number of cancer survivors. The means by which CICI occurs is becoming better understood, but there still remain unsolved questions of the mechanisms involved. The hypotheses to explain CICI are numerous. More than 50% of FDA-approved cancer chemotherapy agents are associated with reactive oxygen species (ROS) that lead to oxidative stress and activate a myriad of pathways as well as inhibit pathways necessary for proper brain function. Oxidative stress triggers the activation of different proteins, one in particular is tumor necrosis factor alpha (TNFα). Following treatment with various chemotherapy agents, this pro-inflammatory cytokine binds to its receptors at the blood-brain barrier and translocates to the parenchyma via receptor-mediated endocytosis. Once in brain, TNFα initiates pathways that may eventually lead to neuronal death and ultimately cognitive impairment. TNFα activation of the c-jun N-terminal kinases (JNK) and Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathways may contribute to both memory decline and loss of higher executive functions reported in patients after chemotherapy treatment. Chemotherapy also affects the brain's antioxidant capacity, allowing for accumulation of ROS. This review expands on these topics to provide insights into the possible mechanisms by which the intersection of oxidative stress and TNFΑ are involved in chemotherapy-induced cognitive impairment.

Indexed as

AnimalsAntineoplastic AgentsBrainChemotherapy-Related Cognitive ImpairmentHumansOxidative StressSignal TransductionTumor Necrosis Factor-alphaAntineoplastic AgentsTumor Necrosis Factor-alphaChemotherapy induced cognitive impairmentNeuronal deathOxidative stress;Pro-inflammatory cytokines

Identifiers

PMID34424346
PMCPMC10561769
OpenAlexW3195673666

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.